Respiratory System Flashcards

Question

Why does gas exchange take place?

Answer 1

Difference in partial pressure of oxygen in atmospheric air (100mg) and in the alveoli (40mg) drives exchange

Answer 2

Bronchomediastinal trunk/system Ascend with the trachea and enter the venous system. Right - Subclavian and lower part of internal jugular Left - Thoracic duct

Answer 3

- Muscular around the edges - Tendonous in the middle Allows more efficient increase in volume of the thorax as it can flatten. Connected to heart by the pericardium so heart also moves down to some degree.

Answer 4

- Inferior vena cava (in tendon as it's low pressure so can't resist other pressure e.g. muscle contraction) (T8) - Oesophagus (T10) in muscle - Descending aorta (T12)

Answer 5

Phrenic nerves, arising from C3,4,5 in the neck.

Answer 6

Phrenic passes hilum anteriorly Vagus passes hilum posteriorly

Answer 7

Ribs move outward, and the sternim is moved superiorly | Diaphragm moves down and flattens

Answer 8

- In forced expiration the muscles push upward | - Abdominal muscles are used in important actions, along with the diaphragm, such as coughing, vomiting etc.

Answer 9

Volume of air expired in one minute (VE) or per minute

Answer 10

The frequency of breathing per minute

Answer 11

The volume of air reaching the respiratory zone

Answer 12

The process of generating ATP either with an excess of oxygen (aerobic) and a shortfall (anaerobic).

Answer 13

Capacity of the airways incapable of undertaking gas exchange

Answer 14

Capacity of airways that should be able to undertake gas exchange but cannot (e.g. hypoperfused alveoli)

Answer 15

Equivalent to the sum of alveolar and anatomical dead space

Answer 16

Deficient ventilation of the lungs; unable to meet metabolic demand (increased PCO2 - acidosis)

Answer 17

Excessive ventilation of the lungs atop of metabolic demand (results in decreased PCO2 - alkalosis)

Answer 18

Increased depth of breathing (to meet metabolic demand)

Answer 19

Decreased depth of breathing (inadequate to meet metabolic demand)

Answer 20

Cessation of breathing (no air movement)

Answer 21

Difficulty breathing

Answer 22

Abnormally slow breathing rate

Answer 23

Abnormally fast breathing rate

Answer 24

Positional difficulty in breathing (when lying down)

Answer 25

- Chest wall has tendency to spring outwards - Lung has a tendency to recoil inwards - Forces are at equilibrium at end-tidal expiration (Functional residual capacity; FRC) which is neutral position of the intact chest - To further inspire (or expire) requires equilibrium to be temporarily imbalanced

Answer 26

- Lungs are surrounded by visceral pleural membrane - Inner surface of chest wall is covered by a parietal pleural membrane - Pleural cavity between them is a fixed volume and contains protein-rich pleural fluid

Answer 27

- Intrapleural bleeding causing a haemothorax | - Perforated chest wall/punctured lung causing a Pneumothorax

Answer 28

The volume of air inspired during normal, relaxed breathing (about 500ml)

Answer 29

The additional air that can be forcible inhales after the inpiration of a normal tidal volume (about 3100ml)

Answer 30

The additional air that can be forcibly exhaled after the expiration of a normal tidal volume (about 1200ml)

Answer 31

The volume of air still remaining in the lungs after the expiratory reserve volume in exhaled (about 1200ml)

Answer 32

The maximum amount of air that can fill the lungs. (about 6000ml) TLC= TV+IRV+ERV+RV

Answer 33

The total amount of air that can be expired after fully inhaling. (about 4800ml) Varies according to age and body size. VC= TV+IRV+ERV

Answer 34

The maximum amount of air that can be inspired. (about 3600ml) IC= TV+IRV

Answer 35

The amount of air remaining in the lungs after a normal expiration. (about 2400ml) FRC= RV+ERV

Answer 36

- Body Size (height and shape) - Sex (male or female) - Disease (pulmonary, neurological) - Age - Fitness (innate, training)

Answer 37

- Negative pressure breathing: Palv is reduced below Patm e.g. healthy breathing - Positive pressure breathing: Patm is increased above Palv e.g.ventilation, CPR

Answer 38

Transmural pressure = P inside - P outside Transrespiratory pressure = pressure across airways, lungs, chest wall - Negative transrespiratory pressure will lead to inspiration - Positive transmural pressure leads to expiration

Answer 39

- Increased volume of thorax, lowers pressure - Air moves into the lungs, down pressure gradient - Recoil of alveoli increases pressure - Air moves out of the lungs, down pressure gradient

Answer 40

- Bronchi and bronchioles - 17 generations - No gas exchange - Typically 150ml in adults FRC - Anatomical dead space

Answer 41

- Alveoli - 7 generations - Gas exchange - Typicall 350 ml in adults - Air reaching here is equivalent to alveolar ventilation

Answer 42

- Alveoli without blood supply - No gas exchange - Typically 0ml in adults - Called alveolar dead space

Answer 43

- Increase: Ventilation | - Decrease: Tracheostomy

Answer 44

Resistance = 8ηl/πr^4 8 x Viscosity x length of tube ----------------------------------------------- π x radius ^4

Answer 45

P(Gas) is proportional to 1/V(Gas) Volume of a gas is inversely proportional to pressure

Answer 46

- Diaphragm has a pulling force in one direction (like syringe) - Other respiratory muscles move upward and outwards (like bucket handle) Both act to increase the volume of the thorax, and decrease the pressure.

Answer 47

- Equal to the independent chest wall + independent lung - Sigmoid function (S shaped) - So larger change in pressure is required to have a small change in volume at the extremes (total lung capacity, residual volume)

Answer 48

Patient wears noseclip 1. Inhale to TLC 2. Wraps lips around mouth piece 3. Exhale as hard and fast as they can 4. Continue exhaling till RV is reached or 6 seconds have passed 5. Visually inspect performance on graph

Answer 49

Restrictive: Lower FVC, lower FEV1, Higher FEV1/FVC ratio, lower forced expiratory time (FET) Obstructive: Lower FVC, much lower FEV1, lower FEV1/FVC ratio, higher gorced expiratoy time (FET) FEV1 = volume expired in 1 minute

Answer 50

Spirometer: 1. Patient wears noseclip 2. Patient inhales to TLC 3. Patient wraps lips round mouthpiece 4. Patient exhales as hard and fast as possible (don't have to reach RC) 5. Repeat twice and use highest

Answer 51

- Gender - Height - Age

Answer 52

Patient wears noseclip 1. Patient wraps lips round mouthpiece 2. Patient completes at least one tidal breath 3. Patient inhales steadily to TLC 4. Patient exhales as hard and fast as possible 5. Exhalation continues to RV 6. Immediately inhales to TLC

Answer 53

- Restrictive: Displaced to the right, shorter, narrower curve - Severe obstructive: Shorter curve, displaced to the left, indented exhalation curve - Mild obstructive: Very slightly shorter curve, displaced to the left, indented exhalation curve

Answer 54

- Variable extrathoracic obstruction: Blocks inhalation. Blunted inspiratory curve, otherwise normal - Variable intrathoracic obstruction: Blocks exhalation. Blunted expiratory curve, otherwise normal - Fixed airway obstruction: Affects both. Blunted inspiratory and expiratory curve, otherwise normal

Answer 55

Gravity favours ventilation and perfusion of the basal lung versus the apical lung

Answer 56

Pressure of a gas mixture is equal to the sum of the partial pressures of gases in that mixture

Answer 57

Molecules diffuse from regions of high concentration to low concentration at a rate proportional to the concentration gradient, the exchange surface area and the diffusion capacity of the gas. It is inversely proportional to the thickness of the exchange surface.

Answer 58

At a constant temperature, the amount of a given gas that dissolves in a given type and volume of liquid is directly proportional to the partial pressure of that gas in equilibrium with that liquid.

Answer 59

At a constant temperature, the volume of a gas is inversely proportional to the pressure of that gas.

Answer 60

At a constant pressure, the volume of a gas in proportional to the temperature of that gas.

Answer 61

- Room air: 78% nitrogen, 21% oxygen, 0.9% argon, 0.04% CO2 - Oxygen therapy: 40% nitrogen, 59% oxygen etc - Smoke/house fire: Less oxygen, more CO2, some CO - High altitude: Same proportions but smaller volume

Answer 62

- Slowed - Warmed - Humidified - Mixed PO2 decreases + PCO2 increases in respiratory airways, PH2O increases n conducting airways

Answer 63

16ml per minute 250mL per minute is requires at rest. To increase this number specialist binding proteins are needed. (Haemoglobin)

Answer 64

- Four monomers; Each a Ferrous iron ion (Fe2+, valency of 2) at centre of tetrapyrrole porphyrin ring, connected to a protein chain. - Genes responsible for coding the globin chain can produce four variants: - Alpha chain (main) - Beta chain (variant of main) - Gamma chain (foetal heamoglobin) - Delta chain - Capable of carrying 4 O2 molecules - 3 Common variants: - HbA (2 alpha, 2 beta); Adult Hb; 98% - HbA2 (2 alpha, 2 delta); Adult Hb; 2% - HbF (2 alpha, 2 gamma) Foetal Hb; trace amounts - Haemoglobin in toxic, and so is carried in red blood cells.

Answer 65

Cooperative binding: - Haemoglobin has a low affinity for oxygen at the beginning - As more O2 binds the affinity increases Allosteric protein: - As O2 binds the structure of the protein changes, and creates a binding site for 2,3-DPG which binds and changes the protein from relaxed to tense, to promote dissociation of O2.

Answer 66

- When Fe2+ is oxidised to Fe3+ valency and cannot bind oxygen - Can cause functional anaemia (i.e. normal Haematocrit, normal PCV but impaired O2 capacity) - Nitrites oxidise Hb into ferric MetHb - Can be genetically caused

Answer 67

- At low PO2 Hb has a low affinity for O2 and so more dissociation (in tissues) - At high PO2 Hb has a high affinity for O2 and so more association (in alveoli)

Answer 68

The partial pressure at which 50% of Hb is saturated. The higher the P50, the lower the affinity for O2.

Answer 69

- Increased temperature - Acidosis - Hypercapnia (high CO2 levels) - Increased 2,3-DPG levels. Happens in exercise, allows more O2 to be released at the same partial pressure.

Answer 70

- Decreased temperature - Alkalosis - Hypocapnia - Decreased 2,3-DPG

Answer 71

- Same shape as normal, but lower total O2 in blood (downward shift) - Less haemoglobin available to carry O2

Answer 72

- Polycythaemia (abnormally high [Hb]) Blood-doping, over production of red blood cells. (increase haematocrit)

Answer 73

- Hb has higher affinity for CO than O2 - CO occupies binding sites, so less O2 circulates - CO changes affinity of Hb for O2, so it is at a higher affinity. The curve moves downward and to the left.

Answer 74

- Greater affinity than adult Hb, so that it can take O2 from mother's blood in the placenta. - Curve is to the left of normal adult Hb

Answer 75

- Single monomer in the muscle - Much greater affinity that adult Hb so it can take O2 from circulating blood and store it - Curve is to the left, not sigmoid but hyperbolic

Answer 76

Before: 5.3kPa (40mmHg) After: 13.5kPa (101mmHg)

Answer 77

- SO2 = 100% - HbO2 = 20.1mL/dL - CDO2 = 0.34mL/dL - CaO2 = 20.4mL/dL

Answer 78

- Bronchiole circulation drains into the pulmonary vein | - So loss of PO2 slightly (97%)

Answer 79

- Isn't enough to sustain life | - Role is changing the affinity of Hb for oxygen

Answer 80

- SO2 = 75% - HbO2 = 15mL/dL - CDO2 = 0.14mL/dL - CaO2 = 15.1mL/dL

Answer 81

Amount of oxygen lost = 5ml/dL 250ml of oxygen per ml/min

Answer 82

- Very soluble, crossed membrane and dissolves into plasma - Some CO2 will move into the red blood cell Most CO2 transported as bicarbonate, HbCO2 more prevalent in mixed venous blood (i.e. when not bound to O2)

Answer 83

- Carbonic anhydrase accelerates reaction of CO2 and H20 - Produces H2CO3 which dissociates - Bicarbonate is moved out of cell, Chloride shift compensates to maintain resting potential (Cl- entry with H20 through AE1 transporter) - Hb bind CO2 at the amine ends of protein chain, to give HbCO2 - H+ binds to amines in the Hb chain to buffer the inside of the erythrocyte

Answer 84

- Slowly binds to water to form carbonic acid (HCO3) - Carbonic acid dissociates into H+ and HCO3- (bicarbonate) - Some H+ will bind to plasma proteins to buffer pH

Answer 85

``` PaCO2 = 5.3 kPa (40mmHg) PvCO2 = 6.1 kPa (46mmHg) ``` ``` CaCO2 = 48.5 mL/dL CvCO2 = 52.4 mL/dL ```

Answer 86

Amount of CO2 gained = 4ml/dL 200ml CO2/min

Answer 87

0.75 seconds

Answer 88

- Pulmonary transit time is shorter - Manages to diffuse in time during exercise - About 0.25 seconds for O2, and less for CO2

Answer 89

- Due to gravity, blood flow is less to the apical area than basal. - Intrapleural pressure at the base of lung is higher (less negative) so it is easier to ventilate. - Ventilation/perfusion ration is low at the base than apical.

Answer 90

- Trachea: Cartilage C shaped rings to allow for oesophagus, divides into two - Bronchi: C shaped cartilage rings to allow for constriction and dilation - Bronchioles: Smooth muscle, connect to alveoli

Answer 91

- Conduit to: conduct O2 to the alveoli, conduct CO2 out of the lung. (gas exchange) - Facilitated by: mechanical stability (cartilage), control of calibre (smooth muscle) and protection and cleansing

Answer 92

- Cartilage sections around outside (not a full ring, as they are offset) - Air way smooth muscle, sometimes with the terminal end of submucosal glands - Blood vessel - Ciliated cells, goblet cells - Mucus and cilia - Airway lumen

Answer 93

- Lining cells e.g. ciliated, intermediate, brush, basal - Contractile cells e.g. smooth muscle (airway and vasculature) - Secretory cells e.g. goblet (epithelium), mucous, serous (glands) - Connective tissue e.g. fibroblast, interstitial cell (elastin, collagen, cartilage) - Neuroendocrine e.g. nerves, ganglia, neuroendocrine cells, neuroepithelisl bodies - Vascular cells e.g. endothelial, pericyte, plasma cell (and smooth musce) - Immune cells e.g. Mast cell, dendritic cell, lymphocyte, eosinophil, macrophage, neutrophil

Answer 94

- When stimulated, the mucin granules (in a highly concentrated form) fuse with the surface of the cell - This forms a pore which attracts water - As more and more water accumulates the mucin granules change to take it on into a liquid form which spreads from the pore onto the surface - The volume of the mucous expands greatly

Answer 95

- Individual components (acini) - Produced by collecting duct, secreted by ciliated duct and spread by cilia - Serous acini at periphery secrete antibacterials and watery mucous - Mucous acini secrete mucus - Glands also secrete water and salts (e.g. Na+, Cl-)

Answer 96

- 9+2 arrangements ( 9 doublets form a ring, and 2 in the middle) - Dynein arms (on doublets) slide over each other causing the backward and forward motion of the cilia - Mitochondria in the cell provide the ATP - About 200 cilia for one ciliated cell - The co-ordinated movement of areas of cilia so that some beat while others recover so that mucus moves along

Answer 97

- Secretion of mucins, water and electrolytes - Movement of mucus by cilia (mucociliary clearance) - Physical barrier - Production of regulatory and inflammatory mediators: - NO (by NO synthase, possibly to control cilia movement) - CO (by hemeoxygenase, may be antibacterial) - Arachidonic acid metabolites e.g. prostaglandins - Chemokines e.g. interleukin-8 - Cytokines e.g. GM-CSF - Proteases

Answer 98

Important for: - Structure - Tone: Calbibre - Contraction and relaxation - Secretion: Some mediators, cytokines, chemokines In inflammation, there is reaction: - e.g. in Asthma, there is hypertrophy due to cell proliferation. Contribute to tone so there is a greater force of contraction. Big upregulation of NOS and COX (to produce NO and prostaglandins), cytokines and chemokines which recruit inflammatory cells.

Answer 99

- 1-5% cardiac output - Perfusion to the tissue is among highest in the body - Bronchial arteries arise from many sites on aorta, intercostal arteries and others - Blood returns from tracheal circulation via systemic veins - Blood returns from bronchial circulation to both sides of the heart via the bronchial and pulmonary veins - Large plexus of vessels underneath the epithelium

Answer 100

- Good gas exchange - Contributes to warming of inspired air - Contributes to humidification of inspired air - Clears inflammatory mediators - Clears inhaled drugs (good/bad, depending on drug) - Supplies airway tissue and lumen with inflammatory cells - Supplies airway tissue and lumen with proteinaceous plasma

Answer 101

- Under normal conditions the post-capillary venules can contract, pulling cells away from each other allowing plasma to leak - Artificially this can be demonstrated by stimulating the sensory neuron (with motor function) innervating it or using inflammatory mediators e.g. histamine from mast cells, platelet activating factor (PAF)

Answer 102

- Nerves: parasympathetic (cholinergic), sensory - Regulatory and inflammatory mediators: histamine, arachidonic acid metabolites (e.g. prostaglandins, leukotrienes), cytokines, chemokines - Proteinases (e.g. neutrophil elastase) - Reactive gas species (e.g. O2-, NO)

Answer 103

Constriction: - Sensory nerves detect foreign object and stimulates parasympathetic reflex - Impulse travels to brainstem (through vagus nerve) - Parasympathetic (cholinergic) motor pathway causes constriction of smooth muscle (also causes mucus secretion and possibly vasodilation) Relaxation: - Sympathetic sensory nerves relay information and synapse at a cervical thoracic ganglion - Efferent nerve releases NO as a transmitter to smooth muscle causing relaxation - Also, sympathetic stimulation of adrenaline release relaxes smooth muscle in airways

Answer 104

- Eosinophils - Neutrophils - Macrophages - Mast cells - T-lymphocytes Structural cells e.g. smooth muscle

Answer 105

- Histamine - Serotonin - Adenosine - Prostaglandins - Leukotrienes - Thromboxan - Platelet activating factor (PAF) - Endothelin - Cytokines - Chemokines - Growth factor - Proteinases - Reactive gas species

Answer 106

- Smooth muscle contraction or relaxation (both airway and vascular) - Secretion (mucins, water etc) - Plasma exudation - Neural modulation - Chemotaxis - Remodelling

Answer 107

- Asthma, Chronic obstructive pulmonary disease (COPD) and cystic fibrosis - Causes airway inflammation, obstruction and remodelling

Answer 108

- Clinical syndrome characterised by increased airway responsiveness to a variety of stimuli (e.g. allergens, emotional upset, cold air etc) - Airway obstruction varies over short periods of time and is reversible (spontaneously or with drugs) - Common symptoms: dyspnoea, wheezing and cough (varying degrees: mild to severe) - Airway inflammation can lead to remodelling: Increased mucus with inflammatory cells embedded in it (eosinophils), thickening of basement membrane, epithelial fragility, increased size of glands and smooth muscle mass, vasodilation, cellular infiltrate of eosinophils. - Airway wall thrown into folds due to bronchi constriction, lumen narrows and fills with mucus

Answer 109

- Epithelial fragility exposes sensory nerves which causes cholinergic reflex - This causes bronchoconstriction and mucus hypersecretion and vasodilation - Inflammatory cells produce mediators and with time there is hypertrophy of smooth muscle, increases plasma exudation, angiogenesis etc. - Fibroblasts add to basement membrane causing thickening

Answer 110

Increases peripherally (almost exponentially)

Answer 111

- Forms a continuous barrier for protection from external environment - Produces secretions to facilitate clearance via mucociliary escalator, and protect underlying cells as well as maintain reduced surface tension (alveolae) - Metabolises foreign and host-derived compounds - Releases mediators - Triggers lung repair process

Answer 112

- Normally: Columna ciliated cells, basal cells and goblet cells - COPD: increase number of goblet cells (hyperplasia) and increased mucus secretion

Answer 113

- found in large, central and small airways - normally 20% of epithelium - synthesise and secrete mucis - In smokers: goblet cell number almost double, secretions increase and are more viscoelastic - This increases the amount of cigarette particles and microorganisms trapped so greater chance of infection

Answer 114

- Found in large, central and small airways - Normally form 80% of epithelium - Cilia beat metasynchonously - In smokers: ciliated cells are depletes, beat asynchronously, found in bronchioles, unable to transport thickened mucus which leads to infection and bronchitis.

Answer 115

- Bronchiolar ciliated cells: increased in smokers and COPD, beat synchronously to move mucus up to epiglottis and clear trapped debris, cells etc - Clara/Club cells: 20% epithelial cells (lower in smokers), secretory cells, detoxification, involved in repair as progenitor cells

Answer 116

- Type 1 epithelial cells: - Large cells (~80μm) - Very thin to allow gas exchange - Type 2 epithelial cells: - Cuboidal, small (~10μm) but highest in number - Secrete surfactant to decrease surface tension - Repair/progenitor cells - Precursor of type 1 cells - Capillary endothelium - Macrophage - Stromal cells (myo) fibroblasts: - Make extracellular matric - Collagen, elastin to give elasticity and compliance - Divide to repair

Answer 117

Holes in the alveoli which regulate the pressure across the lung and allow air to move between alveoli so that pressure is equal.

Answer 118

- Sit in the corners of the alveoli, embedded in the interstium with the apices facing the air - Contain lamellar bodies which store surfactant prior to release onto the air-liquid interface - Surfactant released by type II lowers surface tension and prevents alveolar collapse on expiration

Answer 119

- In emphysema holes form in the alveolar wall - This reduces the surface area of the lung - After damage fibroblasts will try to repair the tissue, leaving fibrotic region which aren't pliable

Answer 120

- Type II cells grouped together because of rapid division - Underneath epithelium fibroblasts increase in number with increased collagen deposition - Exposed basement membrane from type I cell death causes release of growth factors from the fibroblasts and type II cells - Growth factor would stimulate type II cell division and eventual differentiation to replace type I cells

Answer 121

- Necrosis of type I cells - Type II cell proliferation (too much), excessive fibroblast proliferation and increased deposition of collagen and elastin fibres forming more connective tissue

Answer 122

- Antioxidants e.g. glutathione, superoxide dismutase - To neutralise oxygen free radicals inhales e.g. in smokers - Antiproteinases e.g. leukoproteinase inhibitor (SLPI) - To protect against proteases release by leukocytes to kill bacteria - Carry out xenobiotic metabolism e.g. process and detoxify foreign compounds such as carcinogens in cigarette smoke - Contain metabolic enzymes e.g. cytochrome P450, phase I and phase II enzymes

Answer 123

- Macrophages: (major in healthy): clear up debris, live for months to years, respond to multiple stimuli, high % in peripheral lung - Neutrophils: short term, first to be recruited, release mediators, increase greatly in smokers (more so than macrophages) Both have a role in phagocytosis, antibmicrobial defence, synthesis of antioxidants, xenobiotic metabolism. Healthy: 30% neutrophils, 70% macrophages Smokers: 70% neutrophils, 30% macrophages

Answer 124

- Neutrophils produce serine proteinases e.g. neutrophil elastase (NE) - Macrophages produce metalloproteinases e.g. MMP-9 - Substrates include proteins, connective tissue, elastin, collagen - Activate other proteinases (e.g. NE degrades and activates MMP), can inactivate antiproteases (e.g. MMP degrades and inactivates alpha-1-antitrypsin which is an inhibitor of NE) - Activate cytokines.chemokines and other pro-inflammatory mediators

Answer 125

MMP | Neutrophil elastase

Answer 126

- Antimicrobial effects during infection - Generate highly reactive peroxides - Interact with proteins and lipids In chronic: - Inactivate alpha-1 antitrypsin (an NE inhibitor) - Fragment connective tissue

Answer 127

- Chemokines: IL-8 (neutrophils), MCP-1 (macrophages) - Cytokines: IL-1α, IL-6, TNFα (inflammation) - Growth factors: VEGF, FGF, TGFβ (cell survival, repair and remodelling)

Answer 128

- Smoking (biggest) - Asbestos - Radon/radiation - Rare genetic: susceptibility to nicotine addiction, chemical modification of carcinogens.

Answer 129

- Cells have a propensity to become cancerous - Housekeeping genes prevent this e.g. P53 causes apoptosis if the cell becomes uncontrolled - Smoking disrupts the housekeeping genes, so cells are more likely to become cancerous

Answer 130

- Smoking and lung cancer have positive correlation - Passive smoking has been linked to lung cancer, with a dose response - Risk of lung cancer decreases if given up, no matter what age

Answer 131

- Often asymptomatic - Haemoptysis (coughing up blood) - Unexplained or persistent (i.e. more than 3 weeks) - cough - chest/shoulder pain - chest signs - dyspnoea - hoarseness - finger clubbing (acute angle at nail bed) If seen need urgent referral for a chest x-ray

Answer 132

- X-ray, CT | - Biopsy to analyse the pathology of the cancer (from a bronchoscopy)

Answer 133

- Non small cell cancer: Includes squamous (20-40%), adenocarcinoma (20-40%) and large cell (uncommon). Key treatment is surgical removal of tumour, then chemotherapy - Small cell cancer: 20%, Responds to chemotherapy

Answer 134

TNM = tumour characteristics, lymph node characteristics and metastases

Answer 135

- T1a/b: Tumour 3cm but 7cm, invades parietal pleura, chest wall, diaphragm, phrenic nerve, mediastinal pleura, parietal pericardium or in the main bronchus near carina. - T4: Tumous of any size, invades mediastinum, heart, great vessels, trachea, recurrent laryngeal nerve,oesophagus, vertebral body, carnina

Answer 136

- N1: Hilar nodes - N2: Mediastinal nodes - N3: Contralateral side CT then biopsy the lympth node, or PET scan with radioactive glucose to show uptake activity

Answer 137

Has the tumour spread to other organs? M0: no distant metastasis M1: distant metastasis M1a: separate tumour in contralateral lobe M1b: distant metastasis (in extrathoracic organs)

Answer 138

Localised T1, T2 or T3, N1 or N2, M0: - Relatively fit -> aggressive chemotherapy and radiotherapy - Unift -> chemotherapy or palliative care Extensive M1a malignant pleural effusion, N3, M1b: - Relatively fit -> Agressive chemotherapy - Unfit-> Palliative care

Answer 139

Localised T1/T2, N0, M0: - No co-morbidity -> Surgery either lobectomy or pneuomonectomy (removal of lung) - Co-morbidity -> X-ray therapy (DXT) or radiotherapy Extensive: T1 T2, N2, M0: Chemotherapy then surgery or X-ray therapy T3, N0 N1 N2, M0: X-ray therapy, radiotherapy or chemotherapy then supportive care T4, any N, M0: Chemotherapy then X-ray therapy or supportive care

Answer 140

- The earlier the cancer is seen the better the chance of survival as they are more likely to be able to have surgery (70% chance of saving them)

Answer 141

``` Small cell (doubles every 29 days) (then squamous, then adenocarcinoma) ```

Answer 142

- Cytology (cells): found in sputum, bronchial washings, pleural fluid, endoscopic aspiration of tumour/lymph nodes - Histology (tissues): biopsy at bronchoscopy (central tumours), percutaneous CT guided biopsy (peripheral tumours), mediastinoscopy and lymph node biopsy, open biopsy during surgery with immediate results, resection specimen

Answer 143

Arise from variety of cell; epithelial (most common), mesenchymal, lymphoid - Benign tumour: e.g. chondroma. Don't metastasise, can cause local complications e.g. airway obstruction. - Malignant tumour: potential to metastasise, but variable clinical behaviour, commonest are epithelial tumours

Answer 144

- Squamous and small cell linked to smoking more, due to decrease in smoking, prevalence is decreasing - Adenocarcinoma is the cancer most commonly linked to non-smokers, prevalence is increasing

Answer 145

- Normal epithelium adapts to irritation of smoke (hyperplasia) by having squamous cells instead of ciliated (Squamous metaplasia) - No cilia mean no movement of mucus and carcinogens in them - Cells acquire mutation, and become disorganised and proliferate (dysplasia) - Become a carcinoma in situ, and then an invasive carcinoma - Once it is invasive it can invade tissue, lymphatics and the circulation

Answer 146

- Usually in periphery - Proliferation of atypical cells lining the alveolar walls. Increase in size and eventually become invasive. - Carcinoma in situ produces enzymes which invade underlying tissue and it becomes inavsive.

Answer 147

- Increasing incidence (25-40% of lung cancers) - Commoner in far east, females and non-smokers - Peripheral and more often multicentric - Extrathoracic metastases common and early - Histology must show evidence on glandular differentiation

Answer 148

- 25-40% of lung cancers - Closely associated with smoking - Traditionally central arising, from broncial epithelium, but recent increase in peripheral - Local spread, metastasise late

Answer 149

- Poorly differentiated tumours composed of large cells | - Poor prognosis

Answer 150

- 20-25% of tumours - Often central near bronchi - Very close association with smoking - 80% present with advanced disease - Divide very rapidly, mainly nucleus, often necrotic because they've outgrown blood supply - Very chemosensitive BUT very bad prognosis - Paraneoplastic syndromes

Answer 151

Small cell: - Survival 2-4 months if untreated - 10-20 months with current therapy - Chemoradiotherapy (surgery very rare as most have already metastasised) Non-small cell: - Early stage 1: 60% 5 yr survival - Late stage 4: 5% 5 yr survival - 20-30% have early stage tumours suitable for surgical resection - Less chemosensitive

Answer 152

New treatments are targeted more, so better treatments may be available for certain sub-types or may be dangerous for certain sub-types.

Answer 153

- Bronchial obstruction: Can lead to - collapse of lung, shortness of breath - impair drainage of bronchus and so chest infections - Invasion of local structure: - airways - causing haemoptysis, cough. - large vessels - Superior vena cava syndrome: congestion of head and arm oedema, circulatory collapse (emergency) - oesophagus - dysphagia - chest wall - pain - nerves - Homers syndrome (pupil size changes) - Extension through pleura or pericardium: - pleuritisor pericarditis with effusions: breathlessness, cardiac compromise (emergency) - Diffuse lymphatic spread within lung: - Lymphangitis carcinomatosa: shortness of breath, very poor prognosis

Answer 154

Physical effects of metastatic spread: - brain (fits) - skin (lumps) - liver (liver pain, deranged LFTs) - bones (bone pain, fracture) Paraneoplastic syndrome: Systemic effect of tumour due to abnormal expression by tumour cells of factors (e.g. hormones and other factors) not normally expressed by the tissue from which the tumour arose.

Answer 155

Endocrine: - Antidiuretic hormone (ADH): Inappropriate levels of ADH causing hyponatremia (low Na+) especially in small cell carcinoma - Adrenocorticotrophic hormone (ACTH): Cushing's syndrome. especially in small cell carcinoma - Parathyroid hormone-related peptides: Hypercalcaemia. expecially squamous carcinoma - Other: Calcitonin -> hypocalcaemia, Gonadotrophin -> gynecomastia (enlarged male breasts), serotonin -> 'carcinoid syndrome' Non-endocrine: - Haematologic/coagulation defects, skin, muscular other.

Answer 156

Min ventilation = tidal volume x breathing rate Breathing rate = 60/TTOT TTOT = length of one breath

Answer 157

- Frequency of impulses through the Phrenic nerve to the diaphragm and other respiratory muscles controls the strength of contraction - The higher the metabolic need, the higher the frequency of impulses, and therefore the faster and stronger the contractions leading to faster breathing rate and higher inspiratory flow - Other parts of the brain will stop inspiration and stop expiration to go back to the functional residual capacity

Answer 158

Ventilation = VT/TI x TI/TTOT Where: VT/TI = mean inspiratory flow or neural drive and TI/TTOT = fraction of time of respiratory cycle spent on inspiration

Answer 159

- Ventilation rate = 6 - Breathing rate = 15 - Mean inspiratory flow = 0.26

Answer 160

- lower tidal volume - faster breathing rate - breathe using a larger amount of their maximum volume - But these compensate so tidal volume is about the same For Chronic bronchitis, due to greater inefficiency the PCO2 if much higher than normal. The body doesn't react as it has become desensitiised to prevent overworking of the lungs and muscle.

Answer 161

- Involuntary (metabolic) centre in the medulla (bulbo-pontine): responds to metabolic demands for and production CO2 (5.3kPa) - Voluntary (behavioural) centre in the motor area of cerebral cortex: controls breath holding and singing - Metabolic will always override the behavioural (except in children) - Other parts of cortex, not under voluntary control, influence the metabolic centre e.g. emotional response - Limbic system (survival responses e.g. suffocation, hunger, thirst), frontal cortx (emotions) and sensory inputs (e.g pain, startle) may influence the metabolic centre - Sleep also influences the metabolic centre, via the reticular formation

Answer 162

- Diaphragm centre in motor homunculus in the cortex | - As seen in PET scans, that area increases its oxygen consumption to fulfil command

Answer 163

- H+ receptors in the metabolic centre detect PCO2 changes in the ECF (slow) and appropriately send impulses to the respiratory spinal motor neurones (and upper airway muscles) - Impulse frequency infuences rate and strength of contraction of respiratory muscles, therefore impacts ventilation rate in the lung - Carotid bodies (chemoreceptors) detect changes in PCO2 by H+ receptors and contribute 40% to the metabolic control centre's actions - Feedback from carotid bodies, stretch and irritant receptors and muscle spindles and tendon organs influences the metabolic control centre's impulse frequency - Behaviour centre sends impulses directly to respiratory spinal nerves e.g. to sneeze or cough or hold breath. - In NREM sleep of most people the metabolic centre is able to control breathing

Answer 164

- Carotid body (in carotid sinus at junction of internal and external carotid arteries) samples arterial blood - Rapid response system for detecting changes in arterial PCO2 and PO2 - Hypoxia amplifies the H+ receptor

Answer 165

- Almost a pacemaker for respiration - Group of cells in the ventro-cranial medulla, near the 4th ventricle, which are essential in generating the respiratory rhythm. (called 'gasping centre') - Coordination of this complex with other controllers is necessary for a more ordered and responsive respiratory rhythm

Answer 166

- Early inspiratory: intiates inspiratory flow via respiratory muscles - Inspiratory aumenting: (prolong inspiration) may also dilate pharynx, larynx and airways - Late inspiratory: may signal the end of inspiration and 'brake' the start of expiration - Expiratory decrementing: may 'brake' passive expiration by abducting larynx and pharynx - Expiratory augmenting: may activate expiratory muscles when ventilation increases on exercise - Late expiratory: may signal the end of expiration and onset of inspiration, and may dilate the pharynx in preparation for inspiration

Answer 167

- Irritant; leads to coughing or sneezing (i.e. defensive) - CN V: afferents from nose and face - CN IX: afferents from pharynx and larynx - CN X: from bronchi and bronchioles (also stretch) - Hering-Breuer reflex; pulmonary stretch receptors detect lengthening and shortening and terminate inspiration and expiration though it's weak in humans - CN X: afferents from bronchi and bronchioles (also irritant) - Thoracic spinal cord: from chest wall and respiratory muscles (spindles stretch)

Answer 168

Patient breathes into a bag with differing concentrations of O2 and CO2 - In alkalosis (i.e. hyperoxia or too little CO2) increasing Arterial PCO2 increases minute ventilation - In acidosis (i.e. hypoxia or too much CO2) increasing Arterial PCO2 increases minute ventilation at a faster rate

Answer 169

The level of PCO2 required to breath. (only operates in sleep)

Answer 170

The repsonse to PCO2 is much more responsive (a smaller increase will cause a larger effect, i.e. increased ventilation)

Answer 171

- At high altitude both PO2 and PCO2 are lower because the volume of air is less - The body must acclimatise (takes a few days) - Must increase sensitivity to PCO2

Answer 172

[H+] = constant x PaCO2 / HCO3- PaCO2 determined by the lungs (fast) HCO3- determined by the kidneys (slow) Also Strong ion difference: ratio of {Na+, H+} to Cl-

Answer 173

- Increased ventilation to lower PaCO2 and H+ - Renal excretion of weak (lactate and keto) acids - Renal retention of Cl- to reduce the strong ion difference Metabolic causes e.g. uncontrolled diabetes

Answer 174

- Hypoventilation raises PaCO2 and H+ - Renal retention of weak (lactate and keto) acids - Renal excretion of Cl- to increase strong ion difference Causes: too much ingestion of sodium bicarbonate, or diarrhoea

Answer 175

Central: Acute (more common): Metabolic centre poisoning (drugs, anaesthetic) Chronic: Vascular/neoplastic disease of metabolic centre, congenital central hypoventilation syndrome (rare), Obesity hypoventilation syndrome, chronic mountain sickness Peripheral (more common): Acute: muscle relaxant drugs, myasthenia gravis Chronis: neuromuscular with respiratory muscle weakness Chronic obstructive pulmonary disease: mixture of central (won't breathe) and peripheral (can't breathe)

Answer 176

Rarer than hypoventilation - Chronic hypoxaemia - Excess H+ (metabolic causes e.g. ) - Pulmonary vascular disease - Chronic anxiety (psychogenic)

Answer 177

- Subjective - Could be without breath (suspended breathing with emotional cause) - Could be out of breath/too much breathing. Normal e.g. when exercise exceeds a threshold of comfort

Answer 178

- Medical term for breathlessness but with the connotation of discomfort or difficulty - Breathless on rest implies difficulty with inspiration or expiration - Breathless during exercise implies excessive breathing for the task with or without difficulty

Answer 179

- Tightness: difficulty in inspiring due to airway narrowing. Feeling that chest isn't expanding normally - Increased work and effort: breathing at a high minute ventilation, or at a normal minute ventilation but high lung volume, or against an inspiratory or expiratory resistance - Air hunger (worst): sensation of a powerful urge to breath. Mismatch in demand and supply

Answer 180

- Borg scale: 0 to 10 - Visual analogue scale: continuous from not at all to extremely breathless Still ssubjective, but can be used to compare multiple entries from same patient

Answer 181

- Tests strength of behavioural versus metabolic controller - The time can be prolonged by increasing lung volume, lowering PaCO2 or by taking an isoxic/isocapnic breathe (one where there is no gas exchange) near the break point

Answer 182

- Alkalaemia: Refers to raised pH of blood - Acidaemia: Refers to lowered pH of blood - Alkalosis: Describes circumstances that will decrease [H+] and increase pH - Acidosis: Describe circumstances that will increase [H+] and decrease pH

Answer 183

The blood has a very big buffering capacity which happens immediately. There are many molecules in the blood which can either bind to or release H+ depending on what is needed.

Answer 184

-log[H+] = pH | and so [H+] = 10 ^-pH

Answer 185

- Respiratory acid (CO2 + H2O -> H2CO3 -> H+ + HCO3-) - Metabolic acid e.g. pyruvic, lactic etc Respiratory acid contribute 99% of acid which affects pH

Answer 186

0.000000004 Eg/L a 10% increase

Answer 187

``` pH: 7.35 – 7.45. pO2: 10 – 14kPa pCO2: 4.7 – 6.4kPa Base excess (BE): -2 – 2 mmol/l. HCO3: 22 – 26 mmol/l. ```

Answer 188

The ratio between the normal bicarbonate level and the observed

Answer 189

- Normal > 10kPa - Mild hypoxaemia 8-10kPa - Moderate hypoxaemia 6-8kPa - Sever hypoxaemia

Answer 190

- Changes in ventilation can stimulate a RAPID compensatory response to change CO2, elimination and therefore alter pH (for problems in kidney) - Changes in HCO3- and H+ retention/secretion in the kidneys can stimulate a SLOW compensatory response Acidosis will need alkalosis to correct Alkalosis will need acidosis to correct

Answer 191

- Uncompensated: abnormal pH, abnormal PCO2, normal base excess - Partially compensated: abnormal pH, abnormal PCO2, abnormal bases excess - Fully compensated: normal pH, normal PCO2, abnormal base excess

Answer 192

- Hyperventilation (decreased CO2) | - Vomiting (decreased [H+])

Answer 193

- Hypoventilation | - Diarrhoea

Answer 194

- Type of imbalance: Acidosis, alkalosis or normal? - Aetiology of imbalance: respiratory or metabolic (or normal)? - Any homeostatic compensation? uncompensated, partially compensated or fully compensated? - Oxygenation: hypoxaemia, normoxaemia or hyperoxaemia?

Answer 195

``` Neurophysiological pathway: 1. Sensory stimulus 2. Transducer (sensory nerve excitation) 3. Integration in CNS 4. Sensory impression Behavioural pathway: 1. Sensory impression 2. Perception e.g. tolerance of pain 3. Evoked sensation ```

Answer 196

- Crucial defence mechanism protecting the lower respiratory tract from inhaled foreign material and excessive mucous secretion - Usually secondary to mucociliary clearance. Important in lung disease when mucociliary function is impaired and mucous production is increased - Expulsive phase of cough generates high velocity of airflow, facilitated by bronchoconstriction and mucous secretion

Answer 197

- Most numerous on posterior wall of trachea, at main carina and branching points of large airways. Less numerous in more distal airways and none past the respiratory bronchioles - Present in the pharynx and possible other places e.g. eardrums, diaphragm, pleura etc. - Laryngeal and tracheobronchial receptors respond to chemical and mechanical stimuli

Answer 198

Three types: - Slowly adapting stretch receptors - Rapid adapting stretch receptors - C-fibre (chemical) receptors

Answer 199

- 'Free' nerve endings - Found in the larynx, trachea, bronchi and lungs - Small unmyelinated fibres (C) - Chemical irritant stimuli, inflammatory mediators - Release neuropeptide inflammatory mediators; Substance P, Neurokinin A, Calcitonin Gene related peptide.

Answer 200

- Found in the naso-pharynx, larynx, trachea and bronchi - Small myelinated nerve fibres (Aδ) - Mechanical, chemical irritant stimuli and inflammatory mediators

Answer 201

- Located in airways smooth muscle - Myelinated nerve fibres - Predominantly in trachea and main bronchi - Mechanoreceptors (respond to lung inflation)

Answer 202

- Two types of cough receptors: Mechanosensors and Nociceptors - Mechanosensors stimulated by: Mechanical displacement and citric acid - Nociceptors stimulated by: Capsaicin (TRPV1 channel), Bradykinin, Citric acid (TRPV1 channel) and Cinnamaldehyde (TRPA1 channel)

Answer 203

- Starts with inspiration - The glottis closes, causing a rapid increase in pressure - The glottis opens, and the expiratory phase takes place which is when sound is heard

Answer 204

- 2 phases with an initial explosive phase that is the first cough sound, followed by an immediate phase with decreasing sound - An additional third phase called voiced or glottal phase which gives rise to a second cough sound

Answer 205

Oxygen consumption increases in: - orbital frontal cortex - inferior frontal gyrus - anterior insula - superior temporal gyrus - primary motor and somatosensory cortices

Answer 206

Respiratory: - Acute: tracheobronchitis, bronchopneumonia, viral pneumonia, acute-on-chronic bronchitis, pertussis - Chronic: bronchiectasis, tuberculosis, cystic fibrosis - Airway: Asthma, eosinophilic bronchitis, cough variant asthma, chronic bronchitis, COPD, chronic postnasal drip - Parenchymal diseases: interstitial pulmonary fibrosis, emphysema, sarcoidosis - Tumors: bronchogenic carcinoma, alveolar cell carcinoma, benign airway tumors, mediastinal tumors - Aspirated foreign bodies Non-respiratory: - Middle ear pathology - Cardiovascular diseases: left ventricular failure, pulmonary infarction, aortic aneurysm - Other: gastroesophageal reflux, laryngopharyngeal reflux, recurrent microaspiration, endobronchial sutures, obstructive sleep apnea, laryngeal dysfunction - Drugs: Angiotensin-converting enzyme inhibitor medications

Answer 207

- Acute: 3 weeks. Indication of increased cough reflex or disease

Answer 208

- Excitability of afferent nerves increased by chemical mediators e.g. prostaglandin E2 - Increase in receptor numbers e.g. TRPV-1, voltage gated channels - Neurotransmitter increase e.g. neurokinins in brain stem

Answer 209

- Find underlying disease and treat e.g. asthma treated by inhaling corticosteroids - Symptomatic suppressant therapies: Central action - opiates e.g. codeine, morphine. - New: Amitryptiline, gabapentin - Speech pathology management

Answer 210

- Nose: Trigeminal (CN V) - Pharynx: Glossopharyngeal (CN IX), Vagus (X) - Larynx: Vagus (CN X) - Lungs: Vagus (CNX) - Chest wall: Spinal nerves

Answer 211

- PAIN: From the chest wall, in thorax, sensory information travels through spino-thalamic tract from contralateral side. Travels up to the thalamus and then primary somatosensory cortex. Through Aδ and C receptors/fibres via dorsal horn - TOUCH: Sensory pathway travels up to the medulla on the same side, then to contralateral side of the thalamus and somatosensory cortex. Through Aα and Aβ receptors/fibres via dorsal horn.

Answer 212

- Somatic: Localised - Visceral: Difficult to localise, diffuse in character and referred to somatic structures. Pain arising from various viscera in the thoracic cavity and from chest wall is often qualitatively similar and exhibits overlapping patterns of referral, localisation and quality, leading to difficulties in diagnosis.

Answer 213

- Pleuropulmonary disorder: Pleural inflammation e.g. infection, pulmonary embolism, pneumothorax, malignancy e.g. mesothelioma - Tracheobronchitis: Infections, inhalation of irritants - Inflammation or trauma to chest wall: Rib fracture, muscle injury, malignancy, herpes zoster (intercostal nerve pain) - Referred pain: e.g. shoulder-tip pain of diaphragmatic irritation

Answer 214

Cardiovascular: - Myocardial iscaemia/infarction - Pericarditis - Dissecting aneurysm - Aortic valve disease Gastrointestinal disorders: - Oesophageal rupture - Gastrooesopageal reflux - Cholecystitis - Pancreatitis Psychiatric disorders: - Panic disorder - Self-inflicted

Answer 215

- Troublesome, shortness of breath reported by a patient - Occurs at inappropriately low levels of exertion, and limits exercise tolerance - Unpleasant and frightening experience. Can be associated with feelings of impending suffocation - Poor perception of respiratory symptoms and dyspnoea may be life-threatening - Clinical dyspnoea scale from 0-4 (none to severe). Depends of how much activity they can undertake. Borg scale from 0-10.

Answer 216

Impaired pulmonary function: - Airflow obstruction, restriction of lung mechanics, extrathoracic pulmonary restriction, neuromuscular weakness, gas exchange abnormalities Impaired cardiovascular function: - Myocardial disease leading to heart failure, valvular disease, pericardial disease, pulmonary vascular disease, congenital vascular disease Altered central ventilatory drive or perception: - Systemic or metabolic disease, metabolic acidosis, anaemia Physiologic processes e.g. de-conditioning, hypoxic high altitude, pregnancy, severe exercise, being unfit Idiopathic hyperventilation

Answer 217

- Treat the cause - Treatment for dyspnoea is difficult - Options are: bronchodilators, drugs to affect brain e.g. morphine, lung resection, pulmonary rehabilitation (improve general fitness, health and psychological well-being)

Answer 218

Mechanical: URT filtration, mucociliary clearance, cough, surfactant, epithelial barrier Local: BALT, sIgA, lysozyme, transferrin, antiproteinases, alveolar macrophage Systemic: Polymorphocuclear leukocytes, complement, immunoglobulins

Answer 219

- Cilia line the airways (nose, middle ear, sinuses, trachea, bronchi, up to bronchioles) - Tight junctions between epithelial cells form a barrier - Mucus secreted by goblet cells and submucosal glands trap particles and microbes - Cilia beat (15/sec) forward, then pull back in 'recovery' continuously, beating mucus (and microbes in it) up to airway to be swallowed (and lysed in stomach) or coughed up. - Cilia have claws on the surface to catch microbes, and beat in coordination with others

Answer 220

- Very virile bacteria/virus - Weakened host defence: Either congenital or acquired (most common is smoking, viral infection which kills cilia so they have to regrow)

Answer 221

- Haemophilus infuenzae - Hair-like fimbriae which act as anchors to allow them to attach to the epithelial surface - Once attached, it divides and forms a colony on the surface - Symptoms include yellow/green phlegm

Answer 222

- Exoproducts that impair mucociliary clearance: toxins cause cilia to beat in a slow disorganised way, stimulate mucis production, affect ion transport and damage epithelium - Ezymes: break down local immunoglobulins - Exoproducts: impair neutrophil, macrophage and lymphocyte function - Adherence: increased by epithelial damage and tight junction separation - Avoid immune surveillance: surface heterogeneity (changes antigens), biofilm formation, surround gel and endocytosis

Answer 223

- Histologically: solid lung because alveoli are full of pus and inflammatory debris - Very serious, can lead to death - Symptoms: Cough, sputum (yellow), fever, dyspnoea, pleural pain, headache - Commonest cause of bacterial pneumonia: streptococcus pneumoniae - Surrounded by polysaccharide capsule prevents binding to epithelia but allows evasion. Produces toxin pneumolysin which degrades cells.

Answer 224

- Widening of bronchi and their branches due to structural damage, which increases the risk of injection - Low FEV1, Large residual volume, normal gas transfer in aleoli Common complaints: - Large amount of phlegm produced daily - Recurrent respiratory infections - Breathlessness: wheeziness - Fatigue: severe tireness and lethargy, difficulty concentrating Treatment: physiotherapy to learn to cough up phlegm to reduce risk of infection. Treat cause. pulmonary rehabilitation. antibiotics.

Answer 225

- Congenital e.g. pulmonary sequestration, bronchial wall abormalities - Mechanical obstructions e.g. foreign body, tumour, lymph node - Inflammatory pneumonitis e.g. gastric contents, caustic gas - Fibrosis e.g. CFA (ideopathic fibrosis), sarcoid - Postinfective e.g. TB, pneumonia - Immunological e.g. Allergic bronchopulmonary aspergillosis (ABPA), post-transplant - Impaired mucociliary clearance e.g. cystic fibrosis, Primary ciliary dyskinesia (PCD), Youngs syndrome - Immune deficiency e.g. hypogammaglobulinaemia

Answer 226

Impaired lung defences -> microbial infection -> inflammation -> tissue damage -> impaired lung defences and so on

Answer 227

Balance of protease (produced by neutrophils) and antiprotease (produced by epithelium to prevent damage) So much protease is released by the mass of neutrophils there is damage to the epithelial lining. Then leading to further infections due to lack of defences.

Answer 228

Obstructive: Flow of air into and out of the lung is obstructed. - Lungs operate at higher volumes - Smaller inspiratory reserve volume, tidal volume and expiratory reserve volume - Larger residual volume Restrictive: Inflation/deflation of the lung or chest wall is restricted. - Lungs are operating at lower volumes - All volumes are reduced

Answer 229

Obstructive: - Chronic: COPD, Emphysema, Bronchitis - Acute: Asthma Restrictive: - Pulmonary causes: Lung fibrosis, interstitial lung disease - Extrapulmonary causes: Obesity, neuromuscular disease

Answer 230

- Pressure = 0, Volume = 3L - Both atmospheric and alveolar pressure is 0 therefore transmural pressure = 0 - So no air flow

Answer 231

- Tidal volume is slightly higher, Residual volume and functional residual capacity are higher - Smaller in y-axis because of smaller vital capacity - Narrower curve, so with any given change in pressure there is greater change in volume

Answer 232

- Tidal volume, functional residual capacity and residual volume are reduced - Elongated in the x-axis, so if the low and high volumes are to be reached very high/low pressures must be applied

Answer 233

- Before inspiration, alveolar pressure is at 0 and volume is at 0 - During inspiration, alveolar pressure becomes negative (-5 - so higher pressure outside) and volume increases - At the end of inspiration, alveolar pressure is at 0, and volume is at 0.5L - During expiration the lung recoils so the alveolar pressure becomes positive (5 so higher pressure inside) and volume decreases - At the end of expiration alveolar pressure is 0 and volume is 0

Answer 234

The tendency to distort (change shape) under pressure. e.g. condom Compliance = change in volume / change in pressure

Answer 235

The tendency to recoil to it's original shape/volume e.g. balloon Elastance = change in pressure / change in volume

Answer 236

- For a given change in pressure, there is a much greater change in volume. (than air) - Sigmoid shape for volume over pressure. - Fluid-filled lungs are more compliant than air-filled lungs. - Air-water interface exhibits surface tension (more likely to recoil), whereas fluid-water interface does not

Answer 237

The attraction of water in a surface to each other (due to unmet hydrogen forces) which causes curvature.

Answer 238

- Pulmonary surfactant secreted by Type II pneumocytes. - Made of phospholipids, which arrange their hydrophobic and hydrophilic heads and tails to prevent collapse. - Lowers collapsing pressure of smaller alveoli by increasing the surfactant to water ratio - Prevents collapse of small alveoli, increases compliance by reducing surface tension and reduces the work of breathing

Answer 239

- Resistance is inversely proportional to the radius^4 - Conduction is the ability of the airways to allow a larger volume of air through them. (increases with decreasing resistance and increasing volume)

Answer 240

As the number of airways increases (exponentially) the resistance decreases greatly. (radius peaks at 4, then decreases)

Answer 241

- Pre-inspiration: Airway transmural pressure = +5 therefore it is patent (open) - Mid-inspiration: Airway transmural pressure = +6 therefore it is patent (open) - End inspiration: Airway transmural pressure = +8 therefore is it patent (open) - Forced expiration: Airway transmural pressure = -2 therefore it is collapsed

Answer 242

- Upper airways - Allergic rhinitis - Bronchi - asthma - Alveoli - allergic alveolitis (uncommon)

Answer 243

An exaggerated immunological response to a foreign substance (allergen) which is either inhaled, swallowed, injected or comes into contact with the skin or eye. - Mechanism not a disease. - Can be IgE mediated i.e. the atopic diseases hayfever, eczema, asthma - Can be non-IgE mediated allergic diseases e.g. coeliac disease, allergic alveolitis

Answer 244

- Literally means 'Out of place' - Atopy is the hereditary predisposition to produce IgE antibodies against common environmental allergens - Atopic diseases are allergic rhinitis, asthma and atopic eczema - People with this are characterised by infiltration of Th2 cells and eosinophils

Answer 245

ACUTE: Allergen crosslinks IgE antibodies coating mast cells in the blood. Stimulates the energy dependent secretory process and release of mediators e.g. histamine, which cause smooth muscle spasm and vasodilation. Occur after a few minutes of exposure. CHRONIC: If exposed for continuing amount, T-cell mechanism would start and memory cells would become activated. Other mediatory released from Th2 cells e.g. Il-13 and inflammatory cytokines. This would cause the chronic symptoms of allergy.

Answer 246

- IL-4 stimulates IgE synthesis - IL-5 stimulates eosinophil development/maturation - IL-9 stimulate mast cell development - IL-13 stimulates IgE synthesis, airway hyperresponsiveness and increases mucus secretion

Answer 247

The common progression from food allergy, to atopic dermatitis, to asthma and then to allergic rhinitis through childhood.

Answer 248

(Hayfever) Caused by allergy to enzymes in pollen grains.

Answer 249

House dust mite, cats, dogs, Alternaria, Cockroaches, horses

Answer 250

- Narrowing of airways due to inflammation - Due to three things: constriction of smooth muscle, oedema of airway and plugging of small airways (serious) - Some due to allergy some not.

Answer 251

- Early onset allergic : Th2 involved, often an allergy - Late onset eosinophilic: IL-5 involved, not normally an allergy - Exercise-induced: Th2, not an allergy - Obesity-related: no Th2 markers, not an allergy - Neutrophilic: Chronic, Th17/IL-8, not an allergy

Answer 252

- Decrease in blood pressure can cause dizziness or loss of consiousness - Bronchoconstriction - Lip, tongue swelling - Tingling - Arrythmia - Uticaria/hives and others

Answer 253

Sensitivity to substance where minute amounts cause a severe generalised reaction. Caused by activation of mast cells and mass release of histamine.

Answer 254

- Drugs e.g. penicillin - Biggest cause = Food e.g. peanuts, otherr nuts, shellfish etc - Insect stings from bees, wasps, hornets - Latex

Answer 255

Adrenaline

Answer 256

- Farmer's Lung - Caused by inhaling microscopic spores from mouldy hay. The interstitium (area between alveoli and capillary) becomes inflamed which impairs gas exchange. - Severe breathlessness and lung fibrosis etc

Answer 257

- Autoimmune diseases in general have increased - Not due to 'hygiene hypothesis' or pollution - Loss of species diversity - Risk factors: 'Westernised countries', small family size, affluent urban homes, intestinal microflora stable, high antibiotic use, low or absent helminth burden, good sanitation, low orofaecal burden - Lack of exposure to common bacteria stimulates T-regulatory lymphocytes which would prevent over activation of IgE when exposed to other substances

Answer 258

- Allergen avoidance - Anti-allergic medication e.g. antihistamines, bronchodilators, corticosteroids - Immunotherapy (dessensitisation/hyposensitisation) e.g Subcutaneus immunotherapy: injection of increasing amounts of the allergen or Sublingual immunotherapy: same thing but drops under tongue

Answer 259

- Grass and tree pollen allergic rhino-conjunctivitis uncontrolled by medication - Bee or wasp sting anaphylaxis at risk for repeated stings How: - Downregulates Th2 lymphocytes - Increases Th1 lymphocytes - Increases Regulatory T cells

Answer 260

Low PO2 environment.

Answer 261

Low PaO2 in the blood.

Answer 262

Lack of oxygen flowing to tissue.

Answer 263

- Disease e.g. COPD. - Exercise - does not usually result in exercise due to good responses by the body - Altitude

Answer 264

- Atmosphere PO2 = 21.3kPa - In airways PO2 = 20.0kPa - In alveoli PaO2 = 13.5kPa - In pulmonary vein and heart PaO2 = 13.3kPa - In tissues PaO2 = 5.3kPa - In veins PaO2 = 5.3kPa

Answer 265

Steadily decreases because the lung loses some ability to ventilate as well.

Answer 266

The decreasing oxygen tension from inspired air to respiring cells. (diffusion gradient)

Answer 267

- Initially oxygen deficit - When you start exercising the medulla controls breathing, and propioceptive afferent nerve fibres from the skeletal muscles send impulses to the brain to increase breathing - Efferent nerve fibres from the motor cortex to the skeletal muscle also sends impulses to the medulla to increase breathing - Through nervous and metabolic control a steady state is reached - After exercise there is still oxygen consumption to repay oxygen debt e.g. myoglobin re-saturation. Immediate stop of neurogenic control of breathing as there is not motor cortex/muscle stimulation to medulla

Answer 268

- Increased tidal volume intially (as it's the most effective method of increasing ventilation) - Then an increase in breathing rate if necessary - Respiratory frequency stabilises at around 20 breaths per minute

Answer 269

- The volume of oxygen available at each stage is severely decreased - Hypobaric hypoxia (inadequate volume of oxygen)

Answer 270

- Low atmospheric O2 - Lower PAO2 -> Lower PaO2 - Activation of peripheral chemoreceptors - Increased sympathetic outflow -> Increased heart rate and contractility -> increase O2 loading - Increased ventilation - > PAO2 -> Increased O2 loading - Decreased PaCO2 -> decreased central drive to breathe -> decreased ventilation -> decreased O2 loading - Increased pH ---> leftward shift of oxygen dissociation curve -> decreased unloading - Alkalosis detected by carotid bodies -> Increased HCO3- excretion by kidneys -> Increased H+ in blood -> Oxygen dissociation curve normalises -> increased O2 loading - Also low PaO2 -> increased erythropoeitin -> increased rbc -> increased O2 loading - Also increased efficiency of oxidative enzymes (better respiration), increased number of mitochondria, -> increase O2 unloading - Also small increase in 2,3-DPG in rbc -> rightward shift in oxygen dissociation curve -> increased O2 loading

Answer 271

- Aclimation: Like acclimatisation but in an artificial environment e.g. hypobaric chamber. - Drugs e.g. Acetazolamide a Carbonic anhydrase inhibitor which accelerate the slow renal compensation to hypoxia-induced hyperventilation

Answer 272

- Barrel chest - larger total lung capacity, more alveoli and greater capillarisation - Increased haematocrit - greater oxygen carrying capacity of the blood - Larger heart to pump through vasoconstricted pulmonary circulation - Increased mitochondrial density - greater oxygen utilisation at cellular level

Answer 273

- Usually arises in native people where the adaptions go wrong - Pathophysiology: Secondary polycythaemia increases blood viscocity which impedes O2 delivery as it can't travel through capillaries effectively - Symptoms: Cyanosis, fatigue - Consequences: ischaemic tissue damage, heart failure, eventual death - Treatment: no medical treatment. Immediate permanent descent.

Answer 274

- Causes: maladaption to the high-altitude environment. Usually associated with recent ascent - onset within 24 hrs and can last more than a week - Pathophysiology: associated with mild cerebral oedema - Symptoms: nausea, vomiting, irritability, dizziness, insomnia, fatigue, dyspnoea - Consequences: development into HAPE (high altitude pulmonary oedema) and HACE (high altitude cerebral oedema) - Treatment: monitor symptoms. stop ascent, analgesia, fluids, medication (acetazolamide) or hyperbaric O2 therapy. Symptoms tend to subside after 48hrs of increased renal compensation

Answer 275

- High altitude cerebral oedema - Cause: rapid acent or inability to acclimatise - Pathophysiology: vasodilation of vessels in response to hypoxaemia, increases fluid leakage and so intercranial pressure increases - Symptoms: confusion, ataxia (loss of control of body movement), behavioural change, hallucinations, disorientatios - Consequences: irrational behaviour, irreversible neurological damage, coma, death - Treatment: Immediate descent, O2 therapy, hyperbaric O2 therapy, dexamethasone (corticosteroid)

Answer 276

- High altitude pulmonary oedema - Causes: rapid acent or inability to acclimatise - Pathophysiology: vasoconstriction of pulmonary vessels in response to hypoxia, increased pulmonary pressure, permeability and fluid leakage from capillaries leads to accumulation once it exceeds maximum rate of lymph drainage - Symptoms: Dyspnoea, dry cough, bloody sputum, crackling chest sounds - Consequences: impaired gas exchange, impaired ventilatory mechanics - Treatment: Descent, hyperbaric O2 therapy, nifedipine, salmeterol, sildenafil (reduce fluid leakage)

Answer 277

- Failure of pulmonary gas exchange, genereally ventilation/perfusion mismatch - Type 1: Hypoxic respiratory failure PaO2 6.7kPa. Can be caused by decreased CNS drive, pulmonary fibrosis, obesity induced hypoventilation

Answer 278

Acute: Myocardial infarction, pulmonary embolus, severe haemhorrage Chronic: Diabetes, respiratory failure, anaemia, COPD

Answer 279

- Embryonic phase: 0-7 weeks. Lung buds being to form and early branching into main bronchi - Pseudoglandular: 5-17 weeks. All the pre-acinar conducting airways formed (Bronchi and bronchioli) - Canalicular: 16-27 weeks. Respiratory airways and blood gas barrier begin to form - Saccular/Alveolar: 28-40 weeks. Alveoli appear - Post-natal to adolescence: Alveoli multiply and enlarge in size with the chest cavity

Answer 280

- Vasculogenesis though branching morphogenesis. - Blood gas barrier where capillaries form - Alveo and angiogenesis Crucial interaction between circulatory and aiway system e.g. growth hormones etc

Answer 281

- Anomalous pulmonary venous drainage of the right lung to the inferior vena cava, usually close to the junction of the right atrium - Associated right lung and right pulmonary artery hypoplasia, dextrocardia (heart points to the right) and anomalous system arterial supply - Majority of patients have the classical subtype (heart situated to right) which is easier to treat than the opposite.

Answer 282

- 15-17 weeks - Branching morphogenesis of airways into mesenchyme - Pre-acinar airways all present by 17 weeks - Development of cartilage, gland and smooth muscle tissue - continues into canicular phase

Answer 283

- Incomplete rings posteriorly - Irregular plates - Increasingly calcify with age - Can be malacic (soft due to delay of calcification in a new born) - Generalised: laryngotracheomalcia - Localised: malacic segment

Answer 284

- Complete tracheal ring narrows airway greatly. Treatment usually tracheal surgery to open airway with tracheostomy to allow breathing before surgery. - Laryngomalacia where cartilage is too soft. Omega shaped epiglottis; aryepiglottic folds which collapse on inspiration. May require tracheostomy or surgery. Usually self limiting where problems go away with age

Answer 285

- Epithelial cells at tips of lung buds are highly proliferative multipotent progenitor cells - Cell behind the tip divide and differentiate into the various cell types - Communication between epithelial cells in distal branching lung buds and surrounding mesenchyme - Epithelial-mesencymal interaction is essential - Genetic and transcription factors [TTF-1] involved in early bud formation - Complex signallying between growth factors, cytokines and receptors in the regulation of lung growth and differentiation

Answer 286

Inductive: - Fibroblastic GF: branching morphogenesis. - Epithelial GF: epithelial proliferation and differentiation Balanced by Inhibitory: - TGFβ: matrix synthesis, surfactant production, inhibits proliferation of epithelium and blood vessels - Retinoic acid: inhibits branching

Answer 287

- Genetic disorder - Movement disorder of the cilia - Caused by a loss of proteins with are used within the cilia to move - E.g. lack of dynein arms leads to immobile cilia - Increased risk of (chronic) infections due to lack of mucociliary clearance

Answer 288

- A circulation is present at 5 weeks - The pulmonary vessels develop alongside the airways - As the heart develop there is already an arterial and venous supply to the foregut where the lung buds begin branching out in to the mesenchyme to form the lungs

Answer 289

Range from abnormal lung with normal vasculature to normal lung with abnormal vasculature

Answer 290

- Range of severity - Defect in pulmonary mesencyma, abnormal differentiation 5-7th week - Normal blood supply, but can be associated with sequestration - Type 2 most commonly seen (in hospitals) : Multiple small cysts. May be associated with renal agenesis, cardiovascular defects, diaphragmatic hernia and syryngomyelia (formation of cavities in cervical region of spinal cord) - Histologically: bronchiolar epithelium with overgrowth, separated by alveolar tissue which was underdeveloped

Answer 291

- Progressive lobar expansion - Underlying cause: weak cartilage, extrinsic compression, one way valve effect, alveoli over-expand (not disrupted) - Males >females - hyperinflation of alveoli, where air cannot escape - CHD association if the heart is pushed due to pressure

Answer 292

- Abnormal segment which shares visceral pleural covering of normal lung - No communication to tracheobronchial tree - Aberrant blood supply which is catheterised and blocked as a treatment method allowing the segment to die - Occurs more in left lobe that right

Answer 293

- Agenesis: complete absence of lung and vessel. Rare. Associated with other pathologies. Mediastinal shift. - Aplasia: blind ending bronchus, no lung or vessel - Hypoplasia: bronchus and rudimentary lung are present, all elements are reduced in size and number. Underperfused and underventilated. Relatively more common, usually secondary. Usually due to lack of space e.g. hernia, chest wall pathology, oligohydramnios (lack of amniotic fluid), lymphatic or cardiac mass or lact of growth e.g. CTM

Answer 294

- Airway epithelia produce VEGF (vascular endothelial growth factor) which stimulates differentiation of endothelial cells to form capillaries within the mesenchyme, - As well as inhibitory factors to prevent overgrowth

Answer 295

- 16-27 weeks - The airspaces at the periphery enlarge - Thinning of epithelium by underlying capillaries to allow gas exchange - Blood gas barrier required in post-natal life is formed - Epithelial differentiation into type I and II cells - Surfactant first detectable at 24-25 weeks. Babies become VIABLE

Answer 296

- 28-40 weeks - Mesenchymal thins and air spaces develop - Usually able to survive self-ventilating at 8 months - At term there is about one third to one half of the number of adult alveoli

Answer 297

- Septa are very important for increasing surface area - Saccule wall: epithelium on both sides with double capillary network. Myofibroblast and elastin fibres at intervals along the wall - At the places secondary septa develop from wall led by elastin produced by myofibroblast. Capillary lines both sides with matrix between - Capillaries have coalesced to form one sheet of alveolar wall, thinner and longer with less matrix. Muscle and elastin still at tip

Answer 298

- Medical care i.e. ventilation, artificial surfactant are not perfect. - May cause harm - May be introducing future at risk groups of disease

Answer 299

- Volume is small though relative to body weight - All airways are present and differentiated - Normal gas exchange though 33-50% alveoli of adults - Same blood gas barrier as adults - Most arteries and veins present

Answer 300

- Decrease in pulmonary vascular resistance - 10 fold rise in pulmonary blood flow - Arterial lumen increases and wall thins rapidly - Change in cell shape and cytoskeletal organisation, not loss of cells - Once thinning has occured, arteries grow and maintain a relatively thin wall

Answer 301

- Expansion of alveoli dilates arteries: direct physical effect - Expansion stimulates release of vasodilator agents (NO, PGI2) - Inhibition of vasoconstrictors present during fetal life (ET) - Direct effect of oxygen on smooth muscle cells

Answer 302

- Lung volume increases x30 - Airways increase in length and width x2-3 by symmetrical growth - Dysanaptic (mismatched) growth during early period - alveoli grow more than airways (airways are relatively large in infants) - Structural elements of the wall increase - Alveoli increase in number till early adolescent, size and complexity to increase surface area - Arteries, veins and capillaries increase as well

Answer 303

Blood pumped from the right ventricle which circulates the lungs allowing oxygen to diffuse into it and associate with haemoglobin, and then enters the left atrium.

Answer 304

- Arteries: Pulmonary arteries are smaller, have less smooth muscle and a relatively larger lumen - Ventricular thickness: Right ventricle wall is much linner - Circuit length/distance: Pulmonary circulation travels a short distance - Pressure: Much lower pressure systemic

Answer 305

Pulsatile pressures (mmHg) - - Aorta: 120/80 - Pulmonary artery: 25/8

Answer 306

``` Systemic: Cardiac Output: 5 L/min Volume: 4.5 L Mean arterial pressure: 93 Pressure gradient: 92 Resistance: 18.4 ``` ``` Pulmonary: Cardiac output: 5 L/min Volume: 0.5 L Mean arterial pressure: 13 Pressure gradient: 9 Resistance: 1.8 ```

Answer 307

1. Gas exchange (oxygen delivery, carbon dioxide) 2. Metabolism of vasoactive substances: ACE enzyme expressed which reacts to form Angiotensin II and breaks down bradykinin 3. Filtration of blood: Filters the circulation for emboli to prevent damage to the heart, brain and other organs. Small emboli will get eliminated in the pulmonary microcirculation. Larger emboli may get trapped in microcirculation causing local perfusion obstruction or if it gets through then potential sudden death

Answer 308

Pulmonary shunt: Anything that bypasses the exchange surface 1. Bronchial circulation: Blood exits heart through aorta, then travels around bronchial circulation then re enters into the left atrium 2. Foetal circulation: Foramen ovale allows blood to pass between the left and right atria. Ductus arteriosus allows blood to flow from the pulmonary artery to the descending aorta 3. Congenital defect: E.g. ventricular defect allowing mixing of blood

Answer 309

- An increased CO and therefore MAP. This should cause impaired pulmonary function because of oedema from increased fluid leakage. But it doesn't because: - An increase in CO will cause pulmonary artery distension and increased perfusion of hypo-perfused beds so there is a negligible change in MAP. There is minimal fluid leakage and no oedema.

Answer 310

- Zones 1-3 (1 is at apex) in the lung | - Due to resistance and gravity, Zone 3 is the most perfused

Answer 311

- Inspiration compresses alveolar vessels, and expiration compresses extra-alveolar vessels. - During expiration, the pressure in the pleural cavity is high so extra-alveolar vessels are compressed (increased resistance), and alveoli are collapsed so the alveolar vessels are stretched. - At functional residual capacity there is no compression - During inspiration, the alveoli expand compressing alveolar vessels (increased resistance). and low pressure in the pleural cavity mean the extra-alveolar vessels are stretched.

Answer 312

- Response to hypoxia is vasoconstriction - Hypoxia causes closure of O2-sensitive K+ channels - Reduced K+ efflux - Increased membrane potential - Membrane depolarisation causes Ca2+ channels in vascular smooth muscle - Constriction

Answer 313

Beneficial: During foetal development - Blood follows path of least resistance - High-resistance pulmonary circuit means increased flow through shunts - First breath increases alveolar PO2 and dilates pulmonary vessels Detrimental: Chronic obstruction lung diseases - Reduced alveolar ventilation, and air trapping - Increased resistance in pulmonary circuit - Pulmonary hypertension - Right ventricular hypertrophy - Congestive heart failure

Answer 314

- Plasma hydrostatic pressure pushes fluid out of the vessel into the lungs - Interstitial hydrostatic pushes fluid into the tissues (but it non-existent in healthy people) - Plasma oncotic pressure forces fluid down the gradient into the vessel due to plasma proteins - Interstitial oncotic pressure forces fluid into the tissues Net: Small net gain of fluid in the tissues. Lymph vessels will drain the fluid and there will be no effect on the lungs.

Answer 315

Leaking of fluid exceeds the maximal rate of clearance by the lymph. - Mitral valve stenosis: Increased plasma hydrostatic pressure - Hypoproteinaemia: Plasma oncotic pressure reduced so less fluid drawn into vessel - Infection: Protiens in interstium, so larger interstitial oncotic pressure - Cancer: Blockage of lymphatic vessels

Answer 316

- Two types: Non-REM sleep (Stage 1,2,3,4) and REM sleep cycle through all of them - 90 minute cycle, majority in deep sleep then REM sleep. - Usually wake up during REM sleep (when you're more likely to dream)

Answer 317

- Reflex/automatic through the Brainstem - In the Pre-Botzinger complex (in the rostral ventral respiratory group) - Can perpetuate respiratory rhythm independent of the body - Close to CSF (feedback)

Answer 318

- Reflex/automatic through the Brainstem - Voluntary/behavioural through the Motor cortex - Emotional through the Limbic system

Answer 319

- Minute ventilation decreases because tidal volume decreases - PCO2 increases by about 0.5kPa which is ESSENTIAL to breathing (stimulates chemoreceptors) - If CO2 doesn't increase (i.e. goes below apnoeic threshold) there will be central apnoea - During sleep the chemoreceptor sensitivity to CO2 decreases - If healthy, the decreased ventilation doesn't affect the SaO2 - If diseased e.g. COPD, the change will lead to an even lower SaO2 and accumulation of CO2

Answer 320

- There is reduced upper airway muscle activity during sleep (Genioglossus and levator palatini) - Extra luminal pressure (ELP) e.g. gravity and adipose tissue, and negative intra luminal ressure (ILP) i.e. inspiration can result in occlusion of the phalangeal airway during sleep. (obstructive sleep apnoea) - Snoring is caused by turbulent airflow passing through the vocal cords due to narrower airways

Answer 321

- Occlusion of the airway and cessation of breathing during sleep - Increasing prevalence - Associated with increased adipose tissue around the airway - Cycle: sleep -> relaxation of muscles -> apnoea -> arousal -> patent airway -> increased ventilation -> sleep - Often don't know it is happening - Feel fatigued through day, more likely to eat unhealthily which will worsen the cycle

Answer 322

- Obstructive: mechanical problem, more common, still effort to breathe but no airflow - Central: low chemo-sensitivity possibly from birth (congenital hyperventilation syndrome), no effort to breathe

Answer 323

- COPD: Already low SaO2 means the decreased ventilation leads to accumulation CO2. Feel sluggish, possible headache when they wake up. - Heart failure: 30-40%. Some patients hyperventilate due to pulmonary oedema which means the PaCO2 is low and therefore below the apnoeic threshold when asleep. This means they are likely to suffer central sleep apnoea. Prognosis is worse if this is the case.

Answer 324

- RQ is the ratio between Carbon dioxide production and oxygen consumption on the muscles - Above 1 there is anaerobic respiration

Answer 325

- Ratio between Carbon dioxide produced and oxygen consumption at the mouth - Measurable - Should be equal to RQ in a steady state

Answer 326

Physiological measure of the energy cost (and oxygen consumption) of an activity Seated and at rest the average sized human requires: 3.5ml/min/kg of oxygen

Answer 327

- At onset of exercise: stored energy (ATP and creatine phosphate) used for muscular contraction - Inorganic phosphates, ADP and creatine drive oxidative phosphorylation - Krebs cycle and glycolysis increase - Oxygen consumption at the muscle (QO2) increases - Initially CO2 production only slightly increases (buffered as HCO30) but then rises to match O2 consumption

Answer 328

- Amount of oxygen that must be taken in after exercise to repay the O2 deficit at the start of exercise

Answer 329

- Increased heart rate (220 minus age is the maximum) - Increased stroke volume, till maximum then a fall due to reduced time to fill between heart beats - Increase cardiac output (from increased volume first, then increased frequency) - Cardiac output increases by 4-7 fold, and O2 consumption 10-15 fold - Mixed venous saturation typically about 75-80% - Up to 85% of oxygen can be extracted during exercise (increased from normal) - VO2 = Cardiac output x (arterial - venous)O2 content

Answer 330

- Increased ventilation rate (initially from increased tidal volume about 1/2 of vital capacity, then breathing rate) - Good ventilation to perfusion matching - Ventilation rate closely related to VCO2 - Aerobic metabolism: RQ rises towards 1 - Anaerobic metabolism RQ rises above 1. Blood becomes acidotic, at musclular level this means a small increase in dissociation of oxygen at the same PO2 - Lactate -> H+ ions which is buffered by bicarbonate. Increased CO2 -> increased ventilation but when H+>HCO3- then there is hyperventilation

Answer 331

Anaerobic threshold: Point where RQ>1 and anaerobic respiration starts Ventilatory compensation point: Where H+>HCO3- and acidosis drives hyperventilation

Answer 332

- Objective measure of exercise capacity (for diagnosis, test of fitness etc) - Measurements: ECG, BP O2 stats, ABG analysis, spirometry - VO2 peak/plateau is the maximum O2 consumption for the test - O2 pulse = VO2 / heart rate. Plateau indicates decrease in stroke volume and heart disease - RER (ratio of VCO2 and VO2 in mouth) - Anaerobic threshold: excessive CO2 production against VO2 - Breathing reserve. Difference in observed maximum ventilation and maximum voluntary ventilation (40xFEV1) - End-tidal CO2 and O2. Rise during exercise and fall in hyperventilation

Answer 333

(CO2:O2 ratio) - Glucose 1 - Protein 0.82 - Lipids 0.7

Respiratory System Flashcards

(362 cards)